BIOD27H3 Lecture Notes - Membrane Potential, Axon Terminal, Organism

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amaranthcattle725

27 Jun 2011

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Claude bernard: also includes: neurotransmitters, hormones and chemicals. Which demonstrated that skin temp was controlled by. Mechanisms distant from the skin: the demonstration that the curare specifically blocks neuromuscular junction (1856). Causing relaxation of muscles: the demonstration that carbon monoxide blocks the respiration of red blood cells (1857). So how do we understand mammalian physiology: days of bernard = 1800"s to 1900"s didn"t have the appropriate technology, so they studied the organism, sometimes by dissecting www. notesolution. com. 2: genome project was started in 1999 and completed in 2003 and they discovered that each encodes several proteins, apply an integrated approach, requirement for hypothesis, experimental design, e. g choice of the correct system (i. e model) Interpretation: variability between subjects (human studies): age, health, lifestyle, weight, psychological bias: caused by experimenter or subject (if human); placebo, cross over, double blinded, ethical considerations: animal numbers, clinical trials with new drugs. How physiologists use technology to understand how the body works:

Related Questions

A well-studied autoimmune and neuromuscular disease affects the neuromuscular junction of afflicted individuals. It turns out that antibodies attack the ligand receptor found on the skeletal muscle cells and reduces the number of these receptors, leading to weakness in eye muscles, facial muscles and in severe cases affects respiratory muscles.

The name and location of the receptor this disease attacks.

What neurotransmitter binds the affected receptors?

In comparing the monosynaptic pathway for an individual without the disease and with the disease, if the sensory neuron in both individuals received the same stimulus (both in intensity and frequency), would the relative amount of neurotransmitter released at the neuromuscular junction differ? Why or why not (meaning explain using the physiology)? (

Would the end plate potential (EPP) differ in a person without the disease versus someone with this disease? How, explain.]

Given the scenario, what branch of the nervous system does this disease affect, central or peripheral? Somatic, parasympathetic, or sympathetic?

Propose a targeted drug treatment for an individual with this disease that would help to improve the effects of the disease. Said in a different way, what is the mechanism that is failing in this disease, and what could be changed to bring it back to ânormalâ.

sangriakangaroo204

1. As a Nursing student in Advanced Human Anatomy, you were ableto observe a total hip replacement. While the O.R. personnel whereprepping the patient for the surgical procedure, theanesthesiologist assumed (rightly so!) that you had some physiologybackground. As such, she launched into the following proceduralexplanation: The patient will need to be intubated, therefore hewill be given a single dose of the neuromuscular blocking agent,succinylcholine to provide muscular relaxation during the surgeryand to facilitate the insertion of the endotracheal tube. Theanesthesiologist asked you the following:

a) Beginning with depolarization at the neuromuscular junction,describe the normal sequence of events which lead to musclecontraction. (10)

b) What prevents acetylcholine (ACh) from accumulating in theneuromuscular junction and causing a sustained contraction in anormal individual? (3)

c) Succinylcholine acts as a depolarizing agent that preventsrepolarization of the nerve. Therefore, no further ACh is releaseduntil the drug is cleared. Name another site within theneuromuscular junction that might be affected to prevent musclecontraction. (Hint: curare acts by this mechanism) (2)

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BIOD27H3 Lecture Notes - Membrane Potential, Axon Terminal, Organism

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